July 18, 2002
"Treatment of patients with [HIV] inhibitors such as ritonavir can result in increases in CD4+ T-cell counts that are independent of a reduction in HIV-1 viral load," according to Shibani Pati and colleagues working at the University of Maryland and Morgan State University in Baltimore.
Ritonavir has significant anticancer effects unrelated to its HIV-inhibiting abilities, the researchers found. Previously, Pati and coauthors discovered that ritonavir can modulate HIV virulence even without blocking the effects of viral protease. By reducing immune cell activation and apoptosis susceptibility, ritonavir creates a less fertile environment for HIV proliferation, they said.
Similarly, ritonavir treatment alters cytokine production by endothelial cells in ways that reduce the risk of KS development. The antiretroviral agent significantly lowered production of cellular factors that promote tumor angiogenesis, downregulated leukocyte adhesion molecules, and prevented transcriptional activation of the KS-promoting protein nuclear factor-(kappa) B, study data showed.
"Taken together, these data suggest that ritonavir has antineoplastic effects that are independent from its ability to inhibit the HIV protease," Pati and colleagues concluded.